To the Editor: Paoloni and Orchard provided a concise summary of the evidence for injections for soft-tissue injuries,1 but omitted some important references on the mechanism of action of corticosteroids and on prolotherapy.

An important action of corticosteroids is blocking of transmission in nociceptive C-fibres.2 Given the lack of evidence of inflammation in chronically painful tendinopathies,3 this is a more probable mechanism of action than the suppression of inflammation. Paoloni and Orchard correctly report that steroids have only a temporary effect in suppressing soft tissue pain. However, in low back pain, if their use is preceded by manual therapy and exercises they have the potential to give more prolonged relief of pain and disability.4

A recent Swedish randomised controlled trial (RCT) of polidocanol prolotherapy injections for chronic Achilles tendinopathy showed reduced pain and normalisation of ultrasound abnormalities.5 Similarly, a New Zealand case series of glucose prolotherapy injections showed very positive results for the same condition.6 An Australian RCT into prolotherapy for chronic low back pain (average duration, 14 years) showed sustained reductions in pain and disability with glucose prolotherapy injections, although similar results were obtained with saline injections.7 A pilot study of glucose prolotherapy in 24 elite male kicking-sport athletes with chronic groin pain (mean duration, 15.5 months) who had failed physical therapy reported a pain-free state and return to sports in 82% at an average follow-up of 17.2 months.8 This evidence would suggest there is a role for this glucose prolotherapy in managing soft-tissue pain, especially as musculoskeletal pain is one of the major presentations to primary practice in Australia. Training primary care physicians in prolotherapy injection techniques should be a priority in medical education.

In reply: We thank Masters and Yelland for their interest in this topic and their notification of additional references, some of which were published after our article was written.

We stated in our article that “the mechanism of any effect of corticosteroid injections in reducing symptoms in purely degenerative tendinopathies is unknown”, and that only where bursitis or tenosynovitis is present would the implication of an anti-inflammatory effect be appropriate.1 While blocking nociceptive C-fibres in normal tendon is demonstrated in the study quoted by Masters and Yelland,2 we still believe that corticosteroids should be used with caution for any tendinopathy where tendon weakening would be potentially harmful. We agree that corticosteroids have a much greater potential role in low back pain, which is a broad entity involving both soft-tissue and joint disorder.

At the time of writing our article there was a pilot study on polidocanol in painful tendons displaying neovascularisation;3 we thank the authors for advising that a randomised controlled trial has since been published.4 While undoubtedly an exciting new therapy, proponents of polidocanol do not consider its mechanism to be simply a “prolotherapy” effect; they also consider sclerosing the neovessels to be critical, and therefore, that hypertonic glucose (the most commonly recommended prolotherapy agent) may not work as well.

We still maintain that prolotherapy currently lacks evidence of efficacy for the treatment of soft-tissue injury in general, although it is relatively cheap and generally free of side effects. Both chronic low back pain, and chronic groin pain, are multifactorial conditions involving joint/bone abnormality which we considered slightly beyond the scope of an article on soft-tissue injuries. We await further publications on the efficacy of prolotherapy with interest.